ILMU KESEHATAN KULIT DAN

KELAMIN

Konsulen:
dr. Hanny Tanasal,
Sp.KK
VITILIGO
REFER Andhika Norris Frabes (2015-84-017)
Defenition
From Latin word vitellus: veal (pale, pink flesh).
an acquired circumscribed depigmentation, found in all
races;
Characterized by the presence of white macula that
can be extensive.
Can affect the body contains melanocyte cells, such as
hair and eye
Epidemiology
found in 0.1 to 2.9% of world population, at any age,
In America: the prevalence of vitiligo around 1%.
Generally appears after birth, can develop in childhood,
the average age of onset is 10 to 30 years.
Found in both men and women, did not differ
significantly in terms of skin type or race
Etiophatogenesis
Still can not be explained with certainty, some theory:
Genetic
Autoimmune and humoral immune response
Cellular immunity mechanism
Disturbances in Oxidant-Antioxidant System in Vitiligo
Neural
Virus
Clasifcation
Grouped based on the distribution and expansion of the
skin:
Focal
Mucosal
Segmental
Acrofacial
Generalize
Universalis
Clinical Manifestation
Most common form of macular amelanosis vitiligo is
covered with normal skin.
The maculas has a uniform color of white milk or like as
if they invade normal skin.
Circular or linear size, the size of a few millimeters to
centimeters.
Lesions usually extends centrifugally.
Asymptomatic lessions, sometimes the lesions are
often exposed to the sun can feel pain from burns
Clinical Manifestation
May affect all parts of the body without exception,
more often at traumatized or gain exposure to the
suns area
Predilection: the face, dorsum manus, axilla, nipple,
umbilicus, sacrum, inguinal and anogenital areas
Clinical variation of vitiligo:
Trichrome vitiligo
Quadricrhome vitiligo
Inflammatory vitiligo
Diagnose
Clinical evaluasion
A family history of lesions and gray hair that arise early
A history of thyroid disorder, alopecia areata, diabetes
mellitus, and pernicious anemia
Possible precipitating factors, such as stress, emotion,
burning sun, and exposure to chemicals
A history of inflammation, irritation, or skin rashes before
white patches
Physical examination
Skin lesions
The macula with 5mm diameter - 5 cm or more, pale white "chalk" and
circumscript.
The macula emerging may be white hazy, showing the transitional phase.
Distribution: Depigmentation appeared in three common forms.
Focal type characterized by one or more of the macula at a single
location, may be the stage of evolution of other types of vitiligo.
Segmental type characterized by one or more of the macula in one place
or one part of the body.
General mode (most common), characterized by a broad distribution
macular depigmentation, often symmetrical.
 Recommendations from the British Association of Dermatologists
The diagnosis of vitiligo can be directly enforced when it appears the classic
presentation
When atypical presentation, the case should be referred for assessment by a
dermatologist
In adults with vitiligo, blood tests to check thyroid function should be considered
Wood's lamp examination may be used to determine the level and activity of vitiligo,
and monitoring response to therapy
The response to the treatment of vitiligo should be considered in the context of a
history of the disease, given that spontaneous repigmentation can occur but are rare
Physicians should assess the psychological effects and quality of life in patients with
vitiligo
In clinical trials of vitiligo, an improvement in patient quality of life should be the most
important outcome measures
Supporting Examination
Histopathological examination
With hematoxylin eosin staining (HE) seems normal except
not found melanocytes, lymphocytes sometimes found on
the edge of the macula. DOPA to melanocytes negative
reaction on apigmentation area, but increased at the edge
of hiperpigmentation.
Examination of Biochemistry
Histochemical examination of the skin incubated with dopa
showed no tyrosinase. Normal tyrosine levels at plasma and
skin.
 Differential Diagnose
Piebaldism
Tinea versicolor
Pytiriasis alba
Nevus depigmentosis
Management
Sunscreen
Cosmetics camouflage
Topical corticosteroid: corticosteroid mid potent
applied once to twice a day for 6-8 weeks, followed by
a pause without treatment for several weeks
Topical immunomodulator: Topical tacrolimus ointment
0.03 to 0.1 % applied 2 times a day in patients with
localized vitiligo
Topical calsipotriol 0,005%
Management
Pseudocatalase
Systemic corticosteroid: prednisone 20-40 mg daily can
be used in the short term in the acute stage
UVB: UVB narrow band 311-nm twice a week is the
treatment of choice in generalized vitiligo in adults, is
also the second choice after corticosteroid or
calcineurin inhibitors in children.
PUVA: can be administered topically (bath PUVA) or
systemic methoksipsoralen or trioksalen.
Management
L-fenilalanine: Oral phenylalanine (50-100 mg / kg /
day) or topically (10%) combined with sunlight or UVA
and topical corticosteroids
Excimer laser : Xenon chloride excimer laser increases
UVB at 308 nm wavelength has been reported to be
effective for the treatment of localized vitiligo
Surgical: suction blister graft, mini-punch grafting and
transfer pure melanocytes culture or mixture epidermal
culture into the area that has been provided
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